Presynaptic mechanisms underlying post-tetanic potentiation at hippocampal mossy fiber synapses

2019 ◽  
Vol 7 (Suppl. 1) ◽  
pp. A3.36
Author(s):  
Yuji Okamoto
Keyword(s):  
Mossy Fiber ◽  
Presynaptic Mechanisms ◽  
Post Tetanic Potentiation

scholarly journals Presynaptic Current Changes at the Mossy Fiber–Granule Cell Synapse of Cerebellum During LTP

2002 ◽  
Vol 88 (2) ◽  
pp. 627-638 ◽  
Author(s):  
Arianna Maffei ◽  
Francesca Prestori ◽  
Paola Rossi ◽  
Vanni Taglietti ◽  
Egidio D'Angelo
Keyword(s):  
Glutamate Receptor ◽  
Granule Cell ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Presynaptic Terminal ◽  
Mammalian Brain ◽  
Channel Blockers ◽  
Presynaptic Mechanisms ◽  
Terminal Excitability

The involvement of presynaptic mechanisms in the expression of long-term potentiation (LTP), an enhancement of synaptic transmission suggested to take part in learning and memory in the mammalian brain, has not been fully clarified. Although evidence for enhanced vesicle cycling has been reported, it is unknown whether presynaptic terminal excitability could change as has been observed in invertebrate synapses. To address this question, we performed extracellular focal recordings in cerebellar slices. The extracellular current consisted of a pre- (P1/N1) and postsynaptic (N2/SN) component. In ∼50% of cases, N1 could be subdivided into N1a and N1b. Whereas N1a was part of the fiber volley (P1/N1a), N1b corresponded to a Ca2+-dependent component accounting for 40–50% of N1, which could be isolated from individual mossy fiber terminals visualized with fast tetramethylindocarbocyanine perchlorate (DiI). The postsynaptic response, given its timing and sensitivity to glutamate receptor antagonists [N2 was blocked by 10 μM [1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide disodium (NBQX) and SN by 100 μM APV +50 μM 7-Cl-kyn], corresponded to granule cell excitation. N2 and SN could be reduced by 1) Ca2+ channel blockers, 2) decreasing the Ca2+ to Mg2+ ratio, 3) paired-pulse stimulation, and 4) adenosine receptor activation. However, only the first two manipulations, which modify Ca2+ influx, were associated with N1(or N1b) reduction. LTP was induced by θ-burst mossy fiber stimulation (8 trains of 10 impulses at 100 Hz separated by 150-ms pauses). Interestingly, during LTP, both N1 (or N1b) and N2/SN persistently increased, whereas P1 (or P1/N1a) did not change. Average changes were N1 = 38.1 ± 31.9, N2 = 49.6 ± 48.8, and SN = 59.1 ± 35.5%. The presynaptic changes were not observed when LTP was prevented by synaptic inhibition, by N-methyl-d-aspartate and metabotropic glutamate receptor blockage, or by protein kinase C blockage. Moreover, the presynaptic changes were sensitive to Ca2+channel blockers (1 mM Ni2+ and 5 μM ω-CTx-MVIIC) and occluded by K+ channel blockers (1 mM tetraethylammmonium). Thus regulation of presynaptic terminal excitability may take part in LTP expression at a central mammalian synapse.

scholarly journals Transsynaptic modulation of presynaptic short-term plasticity in hippocampal mossy fiber synapses

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
David Vandael ◽  
Yuji Okamoto ◽  
Peter Jonas
Keyword(s):  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Brain Slices ◽  
High Frequency Stimulation ◽  
Short Term Plasticity ◽  
Glutamate Signaling ◽  
Frequency Stimulation ◽  
Post Tetanic Potentiation ◽  
Mossy Fiber Synapse ◽  
Ca3 Neurons

AbstractThe hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit. Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this synaptic connection. It is widely believed that mossy fiber PTP is an entirely presynaptic phenomenon, implying that PTP induction is input-specific, and requires neither activity of multiple inputs nor stimulation of postsynaptic neurons. To directly test cooperativity and associativity, we made paired recordings between single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain slices. By stimulating non-overlapping mossy fiber inputs converging onto single CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly, mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only minimal PTP after combined pre- and postsynaptic high-frequency stimulation with intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels, group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire of synaptic computations, implementing a brake on mossy fiber detonation and a “smart teacher” function of hippocampal mossy fiber synapses.

scholarly journals Retrograde suppression of post-tetanic potentiation at the mossy fiber-CA3 pyramidal cell synapse

eNeuro ◽  
2021 ◽  
pp. ENEURO.0450-20.2021
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo
Keyword(s):  
Pyramidal Cell ◽  
Mossy Fiber ◽  
Post Tetanic Potentiation ◽  
Cell Synapse

scholarly journals Retrograde suppression of post-tetanic potentiation at the mossy fiber-CA3 pyramidal cell synapse

2020 ◽  
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo
Keyword(s):  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Mossy Fiber ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Short Term ◽  
Short Term Plasticity ◽  
Dentate Granule Cells ◽  
Post Tetanic Potentiation ◽  
Frequency Facilitation

ABSTRACTIn the hippocampus, the excitatory synapse between dentate granule cell axons – or mossy fibers (MF) – and CA3 pyramidal cells (MF-CA3) expresses robust forms of short-term plasticity, such as frequency facilitation and post-tetanic potentiation (PTP). These forms of plasticity are due to increases in neurotransmitter release, and can be engaged when dentate granule cells fire in bursts (e.g. during exploratory behaviors) and bring CA3 pyramidal neurons above threshold. While frequency facilitation at this synapse is limited by endogenous activation of presynaptic metabotropic glutamate receptors, whether MF-PTP can be regulated in an activity-dependent manner is unknown. Here, using physiologically relevant patterns of mossy fiber stimulation in acute mouse hippocampal slices, we found that disrupting postsynaptic Ca2+ dynamics increases MF-PTP, strongly suggesting a form of Ca2+-dependent retrograde suppression of this form of plasticity. PTP suppression requires a few seconds of MF bursting activity and Ca2+ release from internal stores. Our findings raise the possibility that the powerful MF-CA3 synapse can negatively regulate its own strength not only during PTP-inducing activity typical of normal exploratory behaviors, but also during epileptic activity.SIGNIFICANCE STATEMENTThe powerful mossy fiber-CA3 synapse exhibits strong forms of plasticity that are engaged during location-specific exploration, when dentate granule cells fire in bursts. While this synapse is well-known for its presynaptically-expressed LTP and LTD, much less is known about the robust changes that occur on a shorter time scale. How such short-term plasticity is regulated, in particular, remains poorly understood. Unexpectedly, an in vivo-like pattern of presynaptic activity induced robust post-tetanic potentiation (PTP) only when the postsynaptic cell was loaded with a high concentration of Ca2+ buffer, indicating a form of Ca2+–dependent retrograde suppression of PTP. Such suppression may have profound implications for how environmental cues are encoded into neural assemblies, and for limiting network hyperexcitability during seizures.

scholarly journals Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Nicholas P Vyleta ◽  
Carolina Borges-Merjane ◽  
Peter Jonas
Keyword(s):  
Granule Cells ◽  
Mossy Fiber ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Short Term ◽  
Short Term Plasticity ◽  
Cell Network ◽  
Post Tetanic Potentiation ◽  
Ca3 Pyramidal Cells ◽  
Ca3 Neurons

Mossy fiber synapses on CA3 pyramidal cells are 'conditional detonators' that reliably discharge postsynaptic targets. The 'conditional' nature implies that burst activity in dentate gyrus granule cells is required for detonation. Whether single unitary excitatory postsynaptic potentials (EPSPs) trigger spikes in CA3 neurons remains unknown. Mossy fiber synapses exhibit both pronounced short-term facilitation and uniquely large post-tetanic potentiation (PTP). We tested whether PTP could convert mossy fiber synapses from subdetonator into detonator mode, using a recently developed method to selectively and noninvasively stimulate individual presynaptic terminals in rat brain slices. Unitary EPSPs failed to initiate a spike in CA3 neurons under control conditions, but reliably discharged them after induction of presynaptic short-term plasticity. Remarkably, PTP switched mossy fiber synapses into full detonators for tens of seconds. Plasticity-dependent detonation may be critical for efficient coding, storage, and recall of information in the granule cell–CA3 cell network.

The Reaction of Brain Structures with OsO4-Zinc-Iodide Stain

1971 ◽  
Vol 29 ◽  
pp. 272-273
Author(s):  
Werner J. Niklowitz
Keyword(s):  
Electron Microscope ◽  
Structural Changes ◽  
Mossy Fiber ◽  
Toxic Metal ◽  
Staining Technique ◽  
Brain Structures ◽  
Oxidase Inhibitor ◽  
Fiber Layer ◽  
Hippocampal Tissue ◽  
Zinc Iodide

After intoxication of rabbits with certain substances such as convulsant agents (3-acetylpyridine), centrally acting drugs (reserpine), or toxic metal compounds (tetraethyl lead) a significant observation by phase microscope is the loss of contrast of the hippocampal mossy fiber layer. It has been suggested that this alteration, as well as changes seen with the electron microscope in the hippocampal mossy fiber boutons, may be related to a loss of neurotransmitters. The purpose of these experiments was to apply the OsO4-zinc-iodide staining technique to the study of these structural changes since it has been suggested that OsO4-zinc-iodide stain reacts with neurotransmitters (acetylcholine, catecholamines).Domestic New Zealand rabbits (2.5 to 3 kg) were used. Hippocampal tissue was removed from normal and experimental animals treated with 3-acetylpyridine (antimetabolite of nicotinamide), reserpine (anti- hypertensive/tranquilizer), or iproniazid (antidepressant/monamine oxidase inhibitor). After fixation in glutaraldehyde hippocampal tissue was treated with OsO4-zinc-iodide stain and further processed for phase and electron microscope studies.

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